Upload
finnea
View
63
Download
1
Tags:
Embed Size (px)
DESCRIPTION
Acute Coronary Syndrome. Sofiya Lypovetska, MD PhD Ternopil State Medical University Ukraine. Scope of Problem. CHD single leading cause of death in United States 1,200,000 new & recurrent coronary attacks per year 38% of those who with coronary attack die within a year of having it - PowerPoint PPT Presentation
Citation preview
Acute Coronary SyndromeAcute Coronary Syndrome
Sofiya Lypovetska, MD PhDSofiya Lypovetska, MD PhDTernopil State Medical UniversityTernopil State Medical University
Ukraine Ukraine
Scope of Problem Scope of Problem
CHD single leading cause of CHD single leading cause of death in United Statesdeath in United States
1,200,000 new & recurrent 1,200,000 new & recurrent coronary attacks per year coronary attacks per year
38% of those who with 38% of those who with coronary attack die within a coronary attack die within a year of having ityear of having it
Annual cost > $300 billionAnnual cost > $300 billion
Expanding Risk FactorsExpanding Risk Factors
SmokingSmokingHypertensionHypertensionDiabetes MellitusDiabetes MellitusDyslipidemiaDyslipidemia– Low HDL < 40Low HDL < 40– Elevated LDL / TGElevated LDL / TG
Family History—event Family History—event in first degree relative in first degree relative >>55 male/65 female55 male/65 female
Age-- Age-- >> 45 for 45 for male/55 for femalemale/55 for femaleChronic Kidney Chronic Kidney DiseaseDiseaseLack of regular Lack of regular physical activityphysical activityObesityObesityLack of Etoh intakeLack of Etoh intakeLack of diet rich in Lack of diet rich in fruit, veggies, fiberfruit, veggies, fiber
• Distruption of coronary artery plaque -> platelet activation/aggregation /activation of coagulation cascade -> endothelial vasoconstriction ->intraluminal thrombus/embolisation -> obstruction -> ACS
• Severity of coronary vessel obstruction & extent of myocardium involved determines characteristics of clinical presentation
Pathophysiology of ACSPathophysiology of ACS
Acute Coronary SyndromesAcute Coronary Syndromes
Similar pathophysiologySimilar pathophysiology
Similar presentation and Similar presentation and early management rulesearly management rules
STEMI requires evaluation STEMI requires evaluation for acute reperfusion for acute reperfusion interventionintervention
Unstable AnginaUnstable Angina
Non-ST-Segment Non-ST-Segment Elevation MI Elevation MI (NSTEMI)(NSTEMI)
ST-Segment ST-Segment Elevation MI Elevation MI (STEMI)(STEMI)
Diagnosis of Acute MIDiagnosis of Acute MI STEMI / NSTEMI STEMI / NSTEMI
At least 2 of the At least 2 of the followingfollowing
Ischemic symptomsIschemic symptomsDiagnostic ECG Diagnostic ECG changeschangesSerum cardiac Serum cardiac marker elevationsmarker elevations
Diagnosis of AnginaDiagnosis of Angina
Typical angina—All three of the followingTypical angina—All three of the followingSubsternal chest discomfortSubsternal chest discomfortOnset with exertion or emotional stressOnset with exertion or emotional stressRelief with rest or nitroglycerinRelief with rest or nitroglycerin
Atypical anginaAtypical angina2 of the above criteria2 of the above criteria
Noncardiac chest painNoncardiac chest pain1 of the above1 of the above
CHARACTERISTICS OF TYPICAL ANGINAL CHEST PAIN CHARACTERISTICS OF TYPICAL ANGINAL CHEST PAIN (ADAPTED FROM ROSEN’S, EMERGENCY MEDICINE)(ADAPTED FROM ROSEN’S, EMERGENCY MEDICINE)
CHARACTERISTICCHARACTERISTIC SUGGESTIVE OF ANGINASUGGESTIVE OF ANGINA LESS SUGGESTIVE OF LESS SUGGESTIVE OF ANGINAANGINA
TYPE OF PAINTYPE OF PAIN DULL DULL PRESSURE/CRUSHING PRESSURE/CRUSHING PAINPAIN
SHARP/STABBINGSHARP/STABBING
DURATIONDURATION 2-5 MIN, <20 MIN2-5 MIN, <20 MIN SECONDSTO SECONDSTO HOURS/CONTINUOUSHOURS/CONTINUOUS
ONSETONSET GRADUALGRADUAL RAPIDRAPID
LOCATION/CHEST WALL LOCATION/CHEST WALL TENDERNESSTENDERNESS
SUBSTERNAL, NOT SUBSTERNAL, NOT TENDER TO PALP.TENDER TO PALP.
LATERAL CHEST LATERAL CHEST WALL/TENDER TO PALP.WALL/TENDER TO PALP.
REPRODUCIBALITYREPRODUCIBALITY WITH WITH EXERTION/ACTIVITYEXERTION/ACTIVITY
WITH WITH BREATHING/MOVINGBREATHING/MOVING
AUTONOMIC SYMPTOMSAUTONOMIC SYMPTOMS PRESENT USUALLYPRESENT USUALLY ABSENTABSENT
ATYPICAL PAINATYPICAL PAIN
RISK FACTORS FOR DEVELOPING ATYPICAL PAIN:RISK FACTORS FOR DEVELOPING ATYPICAL PAIN:Diabetes, females, non white patients, elderly, dementia, no prior history of Diabetes, females, non white patients, elderly, dementia, no prior history of MIMIATYPICAL SYMPTOMS:ATYPICAL SYMPTOMS:GIT symptomsGIT symptomsSyncopeSyncopeSOBSOBPleuritic/positional painPleuritic/positional painChest wall tendernessChest wall tendernessNo chest pain/symptomsNo chest pain/symptoms
NRMI 2 STUDYNRMI 2 STUDY – MI without chest pain -> increased risk of death (23% vs – MI without chest pain -> increased risk of death (23% vs 9%)9%)More complications – hypotension,heart failure, strokeMore complications – hypotension,heart failure, strokeDelayed ED presentation, delayed interventionDelayed ED presentation, delayed intervention
Diagnosis of Unstable AnginaDiagnosis of Unstable Angina
Patients with typical angina - An episode of angina Patients with typical angina - An episode of angina Increased in severity or durationIncreased in severity or durationHas onset at rest or at a low level of exertionHas onset at rest or at a low level of exertionUnrelieved by the amount of nitroglycerin or rest that Unrelieved by the amount of nitroglycerin or rest that had previously relieved the painhad previously relieved the pain
Patients not known to have typical anginaPatients not known to have typical anginaFirst episode with usual activity or at rest within the First episode with usual activity or at rest within the previous two weeksprevious two weeksProlonged pain at restProlonged pain at rest
Unstable Unstable AnginaAngina STEMISTEMI NSTEMINSTEMI
Non occlusive thrombus
Non specific ECG
Normal cardiac enzymes
Occluding thrombus sufficient to cause tissue damage & mild myocardial necrosis
ST depression +/- T wave inversion on ECG
Elevated cardiac enzymes
Complete thrombus occlusion
ST elevations on ECG or new LBBB
Elevated cardiac enzymes
More severe symptoms
Acute ManagementAcute Management
Initial evaluation & Initial evaluation & stabilizationstabilization
Efficient risk Efficient risk stratificationstratification
Focused cardiac Focused cardiac carecare
EvaluationEvaluationEfficient & direct history Efficient & direct history Initiate stabilization interventionsInitiate stabilization interventions
Plan for moving rapidly to Plan for moving rapidly to indicated cardiac careindicated cardiac care
Directed Therapies are
Time Sensitive!
Occurs Occurs simultaneouslsimultaneousl
yy
Chest pain suggestive of ischemiaChest pain suggestive of ischemia
– 12 lead ECG12 lead ECG– Obtain initial Obtain initial
cardiac enzymescardiac enzymes– electrolytes, cbc electrolytes, cbc
lipids, bun/cr, lipids, bun/cr, glucose, coagsglucose, coags
– CXRCXR
Immediate assessment within 10 Minutes
– Establish Establish diagnosisdiagnosis
– Read ECGRead ECG– Identify Identify
complicationscomplications– Assess for Assess for
reperfusionreperfusion
Initial Initial labslabs
and testsand testsEmergent Emergent
carecareHistory History
& & PhysicalPhysical
– IV accessIV access– Cardiac Cardiac
monitoringmonitoring– OxygenOxygen– AspirinAspirin– NitratesNitrates
Focused HistoryFocused HistoryAid in diagnosis and Aid in diagnosis and rule out other causesrule out other causes
– Palliative/Provocative Palliative/Provocative factorsfactors
– Quality of discomfortQuality of discomfort– RadiationRadiation– Symptoms associated Symptoms associated
with discomfortwith discomfort– Cardiac risk factorsCardiac risk factors– Past medical history -Past medical history -
especially cardiacespecially cardiac
Reperfusion Reperfusion questionsquestions
– Timing of Timing of presentationpresentation
– ECG c/w STEMI ECG c/w STEMI – Contraindication to Contraindication to
fibrinolysisfibrinolysis– Degree of STEMI riskDegree of STEMI risk
Targeted PhysicalTargeted PhysicalRecognize factors that Recognize factors that increase riskincrease risk
HypotensionHypotensionTachycardiaTachycardiaPulmonary rales, JVD, Pulmonary rales, JVD, pulmonary edema,pulmonary edema,New murmurs/heart New murmurs/heart soundssoundsDiminished peripheral Diminished peripheral pulsespulsesSigns of strokeSigns of stroke
ExaminationExamination– VitalsVitals– Cardiovascular Cardiovascular
systemsystem– Respiratory Respiratory
systemsystem– AbdomenAbdomen– Neurological Neurological
statusstatus
ECG assessmentECG assessment
ST Elevation or new LBBBST Elevation or new LBBBSTEMISTEMI
Non-specific ECGNon-specific ECGUnstable AnginaUnstable Angina
ST Depression or dynamicST Depression or dynamicT wave inversionsT wave inversions
NSTEMINSTEMI
Normal or non-diagnostic EKGNormal or non-diagnostic EKG
ST Depression or Dynamic T wave ST Depression or Dynamic T wave InversionsInversions
ST-Segment Elevation MIST-Segment Elevation MI
New LBBBNew LBBB
QRS > 0.12 secL Axis deviationProminent S wave V1-V3Prominent R wave 1, aVL, V5-V6 with t-wave inversion
Cardiac markersCardiac markersTroponin ( T, I)Troponin ( T, I)
– Very specific and more Very specific and more sensitive than CKsensitive than CK
– Rises 4-8 hours after Rises 4-8 hours after injuryinjury
– May remain elevated May remain elevated for up to two weeksfor up to two weeks
– Can provide Can provide prognostic informationprognostic information
– Troponin T may be Troponin T may be elevated with renal dz, elevated with renal dz, poly/dermatomyositispoly/dermatomyositis
CK-MB isoenzymeCK-MB isoenzyme
– Rises 4-6 hours after Rises 4-6 hours after injury and peaks at 24 injury and peaks at 24 hourshours
– Remains elevated 36-48 Remains elevated 36-48 hourshours
– Positive if CK/MB > 5% of Positive if CK/MB > 5% of total CK and 2 times total CK and 2 times normalnormal
– Elevation can be Elevation can be predictive of mortalitypredictive of mortality
– False positives with False positives with exercise, trauma, muscle exercise, trauma, muscle dz, DM, PEdz, DM, PE
Prognosis with TroponinPrognosis with Troponin
1.01.7
3.4 3.7
6.0
7.5
012345678
0 to <0.4 0.4 to <1.0 1.0 to <2.0 2.0 to <5.0 5.0 to <9.0 9.0
Cardiac troponin I (ng/ml)
Mor
talit
y at
42
Day
s
831 174 148 134 50 67
%%
%%
%
%
Risk StratificationRisk Stratification
UA or NSTEMIUA or NSTEMI- Evaluate for Invasive - Evaluate for Invasive
vs. conservative vs. conservative treatmenttreatment
- Directed medical - Directed medical therapytherapy
Based on initialBased on initialEvaluation, ECG, andEvaluation, ECG, and
Cardiac markersCardiac markers
- Assess for - Assess for reperfusionreperfusion
- Select & implement - Select & implement reperfusion therapyreperfusion therapy
- Directed medical - Directed medical therapytherapy
STEMI Patient?
YESYES NONO
Cardiac Care Goals Cardiac Care Goals
Decrease amount of myocardial Decrease amount of myocardial necrosisnecrosisPreserve LV functionPreserve LV functionPrevent major adverse cardiac events Prevent major adverse cardiac events Treat life threatening complicationsTreat life threatening complications
STEMI cardiac care STEMI cardiac care STEP 1STEP 1: Assessment: Assessment– Time since onset of symptomsTime since onset of symptoms
– 90 min for PCI / 12 hours for fibrinolysis90 min for PCI / 12 hours for fibrinolysis
– Is this high risk STEMI?Is this high risk STEMI?– KILLIP classificationKILLIP classification– If higher risk may manage with more invasive rxIf higher risk may manage with more invasive rx
– Determine if fibrinolysis candidateDetermine if fibrinolysis candidate– Meets criteria with no contraindicationsMeets criteria with no contraindications
– Determine if PCI candidateDetermine if PCI candidate– Based on availability and time to balloon rxBased on availability and time to balloon rx
Fibrinolysis indicationsFibrinolysis indications
ST segment elevation >1mm in two ST segment elevation >1mm in two contiguous leadscontiguous leadsNew LBBBNew LBBBSymptoms consistent with ischemiaSymptoms consistent with ischemiaSymptom onset less than 12 hrs prior to Symptom onset less than 12 hrs prior to presentationpresentation
Absolute contraindications for fibrinolysis Absolute contraindications for fibrinolysis therapy in patients with acute STEMItherapy in patients with acute STEMI
Any prior ICHKnown structural cerebral vascular lesion (e.g., AVM) Known malignant intracranial neoplasm (primary or metastatic)Ischemic stroke within 3 months EXCEPT acute ischemic stroke within 3 hoursSuspected aortic dissectionActive bleeding or bleeding diathesis (excluding menses)Significant closed-head or facial trauma within 3 months
Relative contraindications for fibrinolysis Relative contraindications for fibrinolysis therapy in patients with acute STEMItherapy in patients with acute STEMI
History of chronic, severe, poorly controlled hypertensionSevere uncontrolled hypertension on presentation (SBP greater than 180 mm Hg or DBP greater than 110 mmHg) History of prior ischemic stroke greater than 3 months, dementia, or known intracranial pathology not covered in contraindicationsTraumatic or prolonged (greater than 10 minutes) CPR or major surgery (less than 3 weeks)Recent (within 2-4 weeks) internal bleedingNoncompressible vascular puncturesFor streptokinase/anistreplase: prior exposure (more than 5 days ago) or prior allergic reaction to these agentsPregnancyActive peptic ulcerCurrent use of anticoagulants: the higher the INR, the higher the risk of bleeding
STEMI cardiac careSTEMI cardiac careSTEP 2STEP 2: Determine preferred reperfusion strategy: Determine preferred reperfusion strategy
FibrinolysisFibrinolysis preferred if: preferred if:– <<3 hours from onset3 hours from onset– PCI not available/delayedPCI not available/delayed
door to balloon > door to balloon > 90min90mindoor to balloon minus door to balloon minus door to needle > 1hrdoor to needle > 1hr
– Door to needle goal Door to needle goal <30min<30min
– No contraindicationsNo contraindications
PCIPCI preferred if:preferred if:– PCI availablePCI available– Door to balloon < 90minDoor to balloon < 90min– Door to balloon minus Door to balloon minus
door to needle < 1hrdoor to needle < 1hr– Fibrinolysis Fibrinolysis
contraindicationscontraindications– Late Presentation > 3 hrLate Presentation > 3 hr– High risk STEMIHigh risk STEMI
Killup 3 or higherKillup 3 or higher– STEMI dx in doubtSTEMI dx in doubt
Medical TherapyMedical TherapyMONA + BAHMONA + BAH
MorphineMorphine (class I, level C)(class I, level C)AnalgesiaAnalgesiaReduce pain/anxiety—decrease sympathetic tone, Reduce pain/anxiety—decrease sympathetic tone, systemic vascular resistance and oxygen demandsystemic vascular resistance and oxygen demandCareful with hypotension, hypovolemia, respiratory Careful with hypotension, hypovolemia, respiratory depressiondepression
OxygenOxygen (2-4 liters/minute) (class I, level C)(2-4 liters/minute) (class I, level C)Up to 70% of ACS patient demonstrate hypoxemiaUp to 70% of ACS patient demonstrate hypoxemiaMay limit ischemic myocardial damage by May limit ischemic myocardial damage by increasing oxygen delivery/reduce ST elevationincreasing oxygen delivery/reduce ST elevation
NitroglycerinNitroglycerin (class I, level B)(class I, level B)Analgesia—titrate infusion to keep patient pain freeAnalgesia—titrate infusion to keep patient pain freeDilates coronary vessels—increase blood flowDilates coronary vessels—increase blood flowReduces systemic vascular resistance and preloadReduces systemic vascular resistance and preloadCareful with recent ED meds, hypotension, Careful with recent ED meds, hypotension, bradycardia, tachycardia, RV infarctionbradycardia, tachycardia, RV infarction
AspirinAspirin (160-325mg chewed & swallowed) (class I, (160-325mg chewed & swallowed) (class I, level A)level A)
Irreversible inhibition of platelet aggregationIrreversible inhibition of platelet aggregationStabilize plaque and arrest thrombusStabilize plaque and arrest thrombusReduce mortality in patients with STEMIReduce mortality in patients with STEMICareful with active PUD, hypersensitivity, bleeding Careful with active PUD, hypersensitivity, bleeding disordersdisorders
Beta-BlockersBeta-Blockers (class I, level A)(class I, level A)14% reduction in mortality risk at 7 days at 23% long 14% reduction in mortality risk at 7 days at 23% long term mortality reduction in STEMIterm mortality reduction in STEMIApproximate 13% reduction in risk of progression to Approximate 13% reduction in risk of progression to MI in patients with threatening or evolving MI MI in patients with threatening or evolving MI symptomssymptomsBe aware of contraindications (CHF, Heart block, Be aware of contraindications (CHF, Heart block, Hypotension)Hypotension)Reassess for therapy as contraindications resolveReassess for therapy as contraindications resolve
ACE-Inhibitors / ARBACE-Inhibitors / ARB (class I, level A)(class I, level A)Start in patients with anterior MI, pulmonary Start in patients with anterior MI, pulmonary congestion, LVEF < 40% in absence of congestion, LVEF < 40% in absence of contraindication/hypotensioncontraindication/hypotensionStart in first 24 hoursStart in first 24 hoursARB as substitute for patients unable to use ACE-IARB as substitute for patients unable to use ACE-I
HeparinHeparin (class I, level C to class IIa, level C) (class I, level C to class IIa, level C)– LMWH or UFHLMWH or UFH (max 4000u bolus, 1000u/hr)(max 4000u bolus, 1000u/hr)
Indirect inhibitor of thrombinIndirect inhibitor of thrombin less supporting evidence of benefit in era of reperfusionless supporting evidence of benefit in era of reperfusionAdjunct to surgical revascularization and thrombolytic / Adjunct to surgical revascularization and thrombolytic / PCI reperfusionPCI reperfusion24-48 hours of treatment24-48 hours of treatmentCoordinate with PCI team (UFH preferred)Coordinate with PCI team (UFH preferred)Used in combo with aspirin and/or other platelet inhibitorsUsed in combo with aspirin and/or other platelet inhibitorsChanging from one to the other not recommendedChanging from one to the other not recommended
Additional medication therapyAdditional medication therapyClopidodrelClopidodrel (class I, level B)(class I, level B)
Irreversible inhibition of platelet aggregationIrreversible inhibition of platelet aggregationUsed in support of cath / PCI intervention or if Used in support of cath / PCI intervention or if unable to take aspirinunable to take aspirin3 to 12 month duration depending on scenario 3 to 12 month duration depending on scenario
Glycoprotein IIb/IIIa inhibitorsGlycoprotein IIb/IIIa inhibitors (class IIa, level B)(class IIa, level B)
Inhibition of platelet aggregation at final Inhibition of platelet aggregation at final common pathwaycommon pathwayIn support of PCI intervention as early as In support of PCI intervention as early as possible prior to PCIpossible prior to PCI
Additional medication therapyAdditional medication therapy
Aldosterone blockersAldosterone blockers (class I, level A) (class I, level A)
– Post-STEMI patients Post-STEMI patients no significant renal failure (cr < 2.5 men or 2.0 for no significant renal failure (cr < 2.5 men or 2.0 for women)women)No hyperkalemis > 5.0No hyperkalemis > 5.0LVEF < 40%LVEF < 40%Symptomatic CHF or DMSymptomatic CHF or DM
STEMI care CCUSTEMI care CCU
Monitor for complications: Monitor for complications: recurrent ischemia, cardiogenic shock, ICH, arrhythmiasrecurrent ischemia, cardiogenic shock, ICH, arrhythmias
Review guidelines for specific management of Review guidelines for specific management of complications & other specific clinical complications & other specific clinical scenariosscenarios
PCI after fibrinolysis, emergent CABG, etc…PCI after fibrinolysis, emergent CABG, etc…
Decision making for risk stratification at Decision making for risk stratification at hospital discharge hospital discharge and/orand/or need for CABG need for CABG
Unstable angina/NSTEMI Unstable angina/NSTEMI cardiac carecardiac care
Evaluate for conservative vs. invasive Evaluate for conservative vs. invasive therapy based upon:therapy based upon:
Risk of actual ACSRisk of actual ACSTIMI risk scoreTIMI risk scoreACS risk categories per AHA guidelinesACS risk categories per AHA guidelines
LowLowIntermediateIntermediate
HighHigh
Assessment Findings indicating HIGH likelihood of ACS
Findings indicating INTERMEDIATE likelihood of ACS in absence of high-likelihood findings
Findings indicating LOW likelihood of ACS in absence of high- or intermediate-likelihood findings
History Chest or left arm pain or discomfort as chief symptomReproduction of previous documented anginaKnown history of coronary artery disease, including myocardial infarction
Chest or left arm pain or discomfort as chief symptomAge > 50 years
Probable ischemic symptomsRecent cocaine use
Physical examination
New transient mitral regurgitation, hypotension, diaphoresis, pulmonary edema or rales
Extracardiac vascular disease
Chest discomfort reproduced by palpation
ECG New or presumably new transient ST-segment deviation (> 0.05 mV) or T-wave inversion (> 0.2 mV) with symptoms
Fixed Q wavesAbnormal ST segments or T waves not documented to be new
T-wave flattening or inversion of T waves in leads with dominant R wavesNormal ECG
Serum cardiac markers
Elevated cardiac troponin T or I, or elevated CK-MB
Normal Normal
Risk Stratification to Determine the Likelihood of Acute Coronary Syndrome
TIMI Risk ScorePredicts risk of death, new/recurrent MI, need for urgent
revascularization within 14 days
ACS risk criteriaACS risk criteria
Low Risk ACSNo intermediate or high risk factors
<10 minutes rest pain
Non-diagnositic ECG
Non-elevated cardiac markers
Age < 70 years
Intermediate Risk ACS
Moderate to high likelihood of CAD
>10 minutes rest pain, now resolved
T-wave inversion > 2mm
Slightly elevated cardiac markers
High Risk ACSElevated cardiac markersNew or presumed new ST depressionRecurrent ischemia despite therapyRecurrent ischemia with heart failureHigh risk findings on non-invasive stress testDepressed systolic left ventricular functionHemodynamic instabilitySustained Ventricular tachycardiaPCI with 6 monthsPrior Bypass surgery
Low risk
High risk
ConservaConservative tive
therapytherapy
Invasive Invasive therapytherapy
Chest Pain Chest Pain centercenter
Intermediate risk
Invasive therapy option Invasive therapy option UA/NSTEMIUA/NSTEMI
Coronary angiography and revascularization within 12 to 48 hours after presentation to EDFor high risk ACS (class I, level A)MONA + BAH (UFH)
Clopidogrel– 20% reduction death/MI/Stroke – CURE trial– 1 month minimum duration and possibly up to 9 months1 month minimum duration and possibly up to 9 months
Glycoprotein IIb/IIIa inhibitorsGlycoprotein IIb/IIIa inhibitors
Conservative Therapy for Conservative Therapy for UA/NSTEMIUA/NSTEMI
Early revascularization or PCI Early revascularization or PCI notnot planned plannedMONA + BAMONA + BAHH (LMW or UFH)(LMW or UFH)
ClopidogrelClopidogrelGlycoprotein IIb/IIIa inhibitorsGlycoprotein IIb/IIIa inhibitors– Only in certain circumstances (planning PCI, elevated Only in certain circumstances (planning PCI, elevated
TnI/T)TnI/T)
Surveillence in hospitalSurveillence in hospital– Serial ECGsSerial ECGs– Serial MarkersSerial Markers
Secondary PreventionSecondary Prevention
DiseaseDisease– HTN, DM, HLPHTN, DM, HLP
BehavioralBehavioral– smoking, diet, physical activity, weightsmoking, diet, physical activity, weight
Cognitive Cognitive – Education, cardiac rehab programEducation, cardiac rehab program
Secondary PreventionSecondary Preventiondisease managementdisease management
Blood PressureBlood Pressure– Goals < 140/90 or <130/80 in DM /CKDGoals < 140/90 or <130/80 in DM /CKD– Maximize use of beta-blockers & ACE-IMaximize use of beta-blockers & ACE-I
LipidsLipids– LDL < 100 (70) ; TG < 200LDL < 100 (70) ; TG < 200– Maximize use of statins; consider fibrates/niacin Maximize use of statins; consider fibrates/niacin
first line for TG>500; consider omega-3 fatty acidsfirst line for TG>500; consider omega-3 fatty acids
DiabetesDiabetes– A1c < 7%A1c < 7%
Secondary preventionSecondary preventionbehavioral interventionbehavioral intervention
Smoking cessationSmoking cessation– Cessation-class, meds, counselingCessation-class, meds, counseling
Physical ActivityPhysical Activity– Goal 30 - 60 minutes dailyGoal 30 - 60 minutes daily– Risk assessment prior to initiationRisk assessment prior to initiation
DietDiet– DASH diet, fiber, omega-3 fatty acidsDASH diet, fiber, omega-3 fatty acids– <7% total calories from saturated fats<7% total calories from saturated fats
Thinking outside the box…Thinking outside the box…
Secondary preventionSecondary preventioncognitivecognitive
Patient educationPatient education– In-hospital – discharge –outpatient In-hospital – discharge –outpatient
clinic/rehabclinic/rehab
Monitor psychosocial impactMonitor psychosocial impact– Depression/anxiety assessment & treatmentDepression/anxiety assessment & treatment– Social support systemSocial support system
Medication Checklist Medication Checklist after ACSafter ACS
Antiplatelet agentAntiplatelet agent– AspirinAspirin** and/or Clopidorgrel and/or Clopidorgrel
Lipid lowering agentLipid lowering agent– StatinStatin**– Fibrate / Niacin / Omega-3 Fibrate / Niacin / Omega-3
Antihypertensive agentAntihypertensive agent– Beta blockerBeta blocker**– ACE-IACE-I**/ARB/ARB– Aldactone Aldactone (as appropriate)(as appropriate)
Prevention news…Prevention news…From 1994 to 2004 the death
rate from coronary heart disease declined 33%... But the actual number of
deaths declined only 18% Getting better with
treatment…But more patients developing
disease –need for primary prevention focus
SummarySummaryACS includes UA, NSTEMI, and STEMIACS includes UA, NSTEMI, and STEMI
Management guideline focusManagement guideline focus– Immediate assessment/intervention Immediate assessment/intervention (MONA+BAH)(MONA+BAH)– Risk stratification Risk stratification (UA/NSTEMI vs. STEMI)(UA/NSTEMI vs. STEMI)– RAPID reperfusion for STEMI RAPID reperfusion for STEMI (PCI vs. (PCI vs.
Thrombolytics)Thrombolytics)– Conservative vs Invasive therapy for Conservative vs Invasive therapy for
UA/NSTEMIUA/NSTEMI
Aggressive attention to secondary Aggressive attention to secondary prevention initiatives for ACS patients prevention initiatives for ACS patients
Beta blocker, ASA, ACE-I, StatinBeta blocker, ASA, ACE-I, Statin
Thank You!Thank You!